Is bone loss a physiological cost of reproduction in the Great fruit-eating bat Artibeus lituratus?

During mammalian pregnancy and lactation, the maternal demand for calcium is increased to satisfy fetus and newborn skeletal growth. In addition to the dietary intake, females use the calcium contained in their bones to supply this increased demand, leading to a decrease in maternal bone mineral content. In reproductive insectivorous female bats, bone loss has been described as a physiological cost of reproduction, due to the reported increased risk of bone fracture. This physiological cost may be the mechanism underlying the conflict between increasing litter size and maintaining wing skeletal integrity, which would help to explain the small litter size of most bat species. If bone loss is a linking cost between reproduction and survival in bats, and most bat species have small litter sizes, one would expect to find a loss of bone and an increasing probability of bone fracture during pregnancy and lactation in other non-insectivorous bats. In this study, we tested for the existence of this cost in the Great-fruit eating bat, Artibeus lituratus. We analyzed trabecular structure, bone strength and bone mineral content for the humerus bone, hypothesizing that bone loss during reproduction in females would increase the risk of fracture. Our results showed a decrease of 22-31% in bone trabecular area in lactating females, rapidly compensated following weaning. Bone strength did not differ among reproductive and non-reproductive groups and seems to be more influenced by bone organic components rather than mineral contents. Since we observed bone loss during reproduction yet the humerus strength seems to be unaffected, we suggest that bone loss may not represent a physiological cost during reproduction for this frugivorous bat

Comparative study of the effects of gallium-aluminum-arsenide laser photobiomodulation and healing oil on skin wounds in wistar rats: a histomorphometric study

The present study compared the effects of gallium-aluminum-arsenide diode laser and healing oil on fibroblasts, blood vessels, and collagen maturation of skin wounds in Wistar rats. Twenty-four male rats weighing 325 ± 27 g were used. Five wounds, 12 mm in diameter, were made on the animals' backs. The rats were randomly divided into four groups with six animals in each group. Control group: saline solution; L30 group: 30 J/cm2 laser; L60 group: 60 J/cm2 laser; Oil group: healing oil. Histomorphometric analysis was performed on the scar tissue removed from the different wounds every 4 d for 20 d. On day 4, there were significantly more fibroblasts in the wounds treated with the laser and the healing oil compared to the controls. On day 8, there were significantly more fibroblasts in the oil group compared to the L30 and L60 groups. On the same day, the quantity of vessels was significantly greater in the L60 group compared to the other groups. On day 16, there was a significant increase in the number of blood vessels in the wounds treated with the 60 J/cm2 laser compared to the other groups. Analysis of the collagen maturation index throughout the experiment showed significantly higher values in the L60 group compared to the other groups at all time points. The healing oil exerted a greater effect on fibroblast proliferation, whereas the 60 J/cm2 laser was more effective in stimulating angiogenesis and scar-tissue maturation

Differential Susceptibility of Germ and Leydig Cells to Cadmium-Mediated Toxicity: Impact on Testis Structure, Adiponectin Levels, and Steroidogenesis

This study investigated the relationship between germ and Leydig cell death, testosterone, and adiponectin levels in cadmium-mediated acute toxicity. Cadmium chloride was administered in a single dose to five groups of rats: G1 (0.9% NaCl) and G2 to G5 (0.67, 0.74, 0.86, and 1.1 mg Cd/kg). After 7 days, the animals were euthanized, and the testosterone and testes were analyzed. Dose-dependent Cd accumulation in the testes was identified. At 0.86 and 1.1 mg/kg, animals exhibited marked inflammatory infiltrate and disorganization of the seminiferous epithelium. While Leydig cells were morphologically resistant to Cd toxicity, massive germ cell death and DNA oxidation and fragmentation were observed. Although numerical density of Leydig cells was unchanged, testosterone levels were significantly impaired in animals exposed to 0.86 and 1.1 mg Cd/kg, occurring in parallel with the reduction in total adiponectins and the increase in high-molecular weight adiponectin levels. Our findings indicated that Leydig and germ cells exhibit differential microstructural resistance to Cd toxicity. While germ cells are a primary target of Cd-induced toxicity, Leydig cells remain resistant to death even when exposed to high doses of Cd. Despite morphological resistance, steroidogenesis was drastically impaired by Cd exposure, an event potentially related to the imbalance in adiponectin production

Low doses of simvastatin potentiate the effect of sodium alendronate in inhibiting bone resorption and restore microstructural and mechanical bone properties in glucocorticoid-induced osteoporosis

By using an experimental model of dexamethasone-induced osteoporosis we investigated the effects of different therapeutic schemes combining sodium alendronate (SA) and simvastatin on bone mineral and protein composition, microstructural and mechanical remodeling. Wistar rats were randomized into eight groups: G1: non-osteoporotic; G2: osteoporotic; G3, G4, and G5: osteoporotic + SA (0.2, 0.4, and 0.8 mg/kg, respectively); G6, G7, and G8: osteoporotic + SA (0.2, 0.4, and 0.8 mg/kg, respectively) + simvastatin (0.4, 0.6, and 1 mg/kg, respectively). Osteoporosis was induced by dexamethasone (7 mg/kg, i.m.) once a week for 5 weeks. All treatments were administered for 8 weeks. Dexamethasone increased serum levels of alkaline phosphatase, calcium, phosphorus, and urea, especially in non-treated animals, which showed severe osteoporosis. Dexamethasone also induced bone microstructural fragility and reduced mechanical resistance, which were associated with a marked depletion in mineral mass, collagenous and non-collagenous protein levels in cortical and cancellous bone. Although SA has attenuated osteoporosis severity, the effectiveness of drug therapy was enhanced combining alendronate and simvastatin. The restoration in serum parameters, organic and inorganic bone mass, and mechanical behavior showed a dose-dependent effect that was potentially related to the complementary mechanisms by which each drug acts to induce bone anabolism, accelerating tissue repair

Doxycycline Hyclate Modulates Antioxidant Defenses, Matrix Metalloproteinases, and COX-2 Activity Accelerating Skin Wound Healing by Secondary Intention in Rats

The main objective of this study was to investigate the action of doxycycline hyclate (Dx) in the skin wound healing process in Wistar rats. We investigated the effect of Dx on inflammatory cell recruitment and production of inflammatory mediators via in vitro and in vivo analysis. In addition, we analyzed neovascularization, extracellular matrix deposition, and antioxidant potential of Dx on cutaneous repair in Wistar rats. Male animals (n=15) were divided into three groups with five animals each (protocol: 72/2017), and three skin wounds (12 mm diameter) were created on the back of the animals. The groups were as follows: C, received distilled water (control); Dx1, doxycycline hyclate (10 mg/kg/day); and Dx2, doxycycline hyclate (30 mg/kg/day). The applications were carried out daily for up to 21 days, and tissues from different wounds were removed every 7 days. Our in vitro analysis demonstrated that Dx led to macrophage proliferation and increased N-acetyl-β-D-glucosaminidase (NAG) production, besides decreased cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and metalloproteinases (MMP), which indicates that macrophage activation and COX-2 inhibition are possibly regulated by independent mechanisms. In vivo, our findings presented increased cellularity, blood vessels, and the number of mast cells. However, downregulation was observed in the COX-2 and PGE2 expression, which was limited to epidermal cells. Our results also showed that the downregulation of this pathway benefits the oxidative balance by reducing protein carbonyls, malondialdehyde, nitric oxide, and hydrogen peroxide (H2O2). In addition, there was an increase in the antioxidant enzymes (catalase and superoxide dismutase) after Dx exposure, which demonstrates its antioxidant potential. Finally, Dx increased the number of types I collagen and elastic fibers and reduced the levels of MMP, thus accelerating the closure of skin wounds. Our findings indicated that both doses of Dx can modulate the skin repair process, but the best effects were observed after exposure to the highest dose

Purinergic Antagonist Suramin Aggravates Myocarditis and Increases Mortality by Enhancing Parasitism, Inflammation, and Reactive Tissue Damage in Trypanosoma cruzi-Infected Mice

Suramin (Sur) acts as an ecto-NTPDase inhibitor in Trypanosoma cruzi and a P2-purinoceptor antagonist in mammalian cells. Although the potent antitrypanosomal effect of Sur has been shown in vitro, limited evidence in vivo suggests that this drug can be dangerous to T. cruzi-infected hosts. Therefore, we investigated the dose-dependent effect of Sur-based chemotherapy in a murine model of Chagas disease. Seventy uninfected and T. cruzi-infected male C57BL/6 mice were randomized into five groups: SAL = uninfected; INF = infected; SR5, SR10, and SR20 = infected treated with 5, 10, or 20 mg/kg Sur. In addition to its effect on blood and heart parasitism, the impact of Sur-based chemotherapy on leucocytes myocardial infiltration, cytokine levels, antioxidant defenses, reactive tissue damage, and mortality was analyzed. Our results indicated that animals treated with 10 and 20 mg/kg Sur were disproportionally susceptible to T. cruzi, exhibiting increased parasitemia and cardiac parasitism (amastigote nests and parasite load (T. cruzi DNA)), intense protein, lipid and DNA oxidation, marked myocarditis, and mortality. Animals treated with Sur also exhibited reduced levels of nonprotein antioxidants. However, the upregulation of catalase, superoxide dismutase, and glutathione-S-transferase was insufficient to counteract reactive tissue damage and pathological myocardial remodeling. It is still poorly understood whether Sur exerts a negative impact on the purinergic signaling of T. cruzi-infected host cells. However, our findings clearly demonstrated that through enhanced parasitism, inflammation, and reactive tissue damage, Sur-based chemotherapy contributes to aggravating myocarditis and increasing mortality rates in T. cruzi-infected mice, contradicting the supposed relevance attributed to this drug for the treatment of Chagas disease